FTLD-TDP With and Without GRN Mutations Cause Different Patterns of CA1 Pathology.


Journal

Journal of neuropathology and experimental neurology
ISSN: 1554-6578
Titre abrégé: J Neuropathol Exp Neurol
Pays: England
ID NLM: 2985192R

Informations de publication

Date de publication:
01 09 2019
Historique:
received: 23 03 2019
revised: 03 06 2019
accepted: 20 06 2019
pubmed: 31 7 2019
medline: 19 6 2020
entrez: 31 7 2019
Statut: ppublish

Résumé

Heterozygous loss-of-function mutations in the GRN gene lead to progranulin (PGRN) haploinsufficiency and cause frontotemporal lobar degeneration with TDP-43 pathology type A (FTLD-TDP type A). PGRN is a highly conserved, secreted glycoprotein and functions in the central nervous system as a key modulator of microglial function. Hence, altered microglial function caused by PGRN deficiency may be tied to the pathogenesis of FTLD-TDP. Our previous studies showed that haploinsufficiency of GRN mutations extends to microglial PGRN expression in the hippocampal CA1 region. In this study, we found that the CA1 sector was associated with less neuronal loss and more frequent TDP-43 inclusions in FTLD-TDP type A cases with GRN mutations than in sporadic cases. In addition, the CA1 region in GRN mutation cases contained more rod-like microglia, which also had reduced PGRN expression. These findings suggest that the profile of TDP-43 inclusions, neuronal number, and microgliosis in the CA1 sector of FTLD-TDP type A cases may be influenced by GRN gene expression status.

Identifiants

pubmed: 31361008
pii: 5540708
doi: 10.1093/jnen/nlz059
pmc: PMC7967835
doi:

Substances chimiques

DNA-Binding Proteins 0
GRN protein, human 0
Progranulins 0
TARDBP protein, human 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

844-853

Subventions

Organisme : NIA NIH HHS
ID : P30 AG013854
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG056258
Pays : United States
Organisme : NIDCD NIH HHS
ID : R01 DC008552
Pays : United States
Organisme : NINDS NIH HHS
ID : R35 NS097261
Pays : United States

Informations de copyright

© 2019 American Association of Neuropathologists, Inc. All rights reserved.

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Auteurs

Qinwen Mao (Q)

Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Xiaojing Zheng (X)

Laboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi, P.R. China.

Tamar Gefen (T)

Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Emily Rogalski (E)

Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Callen L Spencer (CL)

Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Rosa Rademakers (R)

Department of Neuroscience, Mayo Clinic, Jacksonville, Florida.

Angela J Fought (AJ)

Division of Biostatistics, Department of Preventive Medicine, Northwestern University Feinberg School of Medicine.

Missia Kohler (M)

Cook County Medical Examiner, Chicago, Illinois.

Sandra Weintraub (S)

Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Haibin Xia (H)

Laboratory of Gene Therapy, Department of Biochemistry, College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi, P.R. China.

Marek-Marsel Mesulam (MM)

Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Eileen H Bigio (EH)

Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Mesulam Center for Cognitive Neurology and Alzheimer's Disease, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

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